Please use this identifier to cite or link to this item:
Title: Agomelatine protects against permanent cerebral ischaemia via the Nrf2-HO-1 pathway
Authors: Wijitra Chumboatong
Satchakorn Khamchai
Chainarong Tocharus
Piyarat Govitrapong
Jiraporn Tocharus
Keywords: Pharmacology, Toxicology and Pharmaceutics
Issue Date: 5-May-2020
Abstract: © 2020 Elsevier B.V. Stroke is a major cause of death and permanent disability worldwide. It has been reported that 85% of stroke patients undergo an ischaemic stroke. The standard treatment is currently recanalization. However, only 5% of patients have access to this treatment. Therefore, new strategies for permanent ischaemic stroke treatment need to be investigated. Agomelatine is a melatonergic agonist that acts on MT1/2 receptors and is an antagonist of 5-HT2c receptors, and melatonergic has pleiotropic effects, such as antioxidation or anti-inflammation effects. In this study, we focused on the effect of agomelatine on permanent cerebral ischaemia in a rat model. Male Wistar rats were randomly divided into the following four groups (n = 6/group): sham operating group, permanent ischaemic model group, permanent ischaemic model plus agomelatine (40 mg/kg, i.p) group and permanent ischaemic model plus melatonin (10 mg/kg, i.p) group. Twenty-four h after ischaemic onset, we investigated the neurological deficits and infarct volume using neurological deficit scores, 2,3,5-triphenyltetrazolium chloride (TTC) and transmission electron microscopy (Kochanski et al.). Moreover, we analysed Nrf2-HO-1 protein expression by Western blot. The results showed that agomelatine and melatonin decreased neuronal injury and promoted the Nrf2-HO-1 signalling pathway. These findings suggest that agomelatine and melatonin exert beneficial effects on permanent cerebral ischaemia.
ISSN: 18790712
Appears in Collections:CMUL: Journal Articles

Files in This Item:
There are no files associated with this item.

Items in CMUIR are protected by copyright, with all rights reserved, unless otherwise indicated.